# ACSL3

Source: https://onco.cc/targets/acsl3/  
OnCo record `acsl3` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

ACSL3 (Fatty acid CoA ligase Acsl3) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Acute myeloid leukaemia.

## Summary

Acyl-CoA synthetases (ACSL) activates long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Required for the incorporation of fatty acids into phosphatidylcholine, the major phospholipid located on the surface of VLDL (very low density lipoproteins). Has mainly an anabolic role in energy metabolism.

Open Targets scores its association with cancer at 0.57 (direct and indirect evidence; datatypes literature 0.98, genetic association 0.00, somatic mutation 0.73). IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Acute Myeloid Leukaemia.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: acyl-CoA synthetase long chain family member 3; Fatty acid CoA ligase Acsl3; ACS3; PRO2194; FACL3
- Tags: cancer-genes-wave
- Symbol: ACSL3
- Class: oncogene
- Biology: Acyl-CoA synthetases (ACSL) activates long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Required for the incorporation of fatty acids into phosphatidylcholine, the major phospholipid located on the surface of VLDL (very low density lipoproteins). Has mainly an anabolic role in energy metabolism. Mediates hepatic lipogenesis. Preferentially uses myristate, laurate, arachidonate and eicosapentaenoate as substrates. Both isoforms exhibit the same level of activity. Location: Mitochondrion outer membrane; Peroxisome membrane; Microsome membrane; Endoplasmic reticulum membrane (UniProt). Locus 2q36.1 (HGNC).
- Where found: Acute myeloid leukaemia: IntOGen driver in 1 cohort (AML)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it an activating (Act) driver in 1 cohort. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:3570: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:3570
- UniProt O95573: https://www.uniprot.org/uniprotkb/O95573/entry
- NCBI Gene 2181: https://www.ncbi.nlm.nih.gov/gene/2181
- Ensembl ENSG00000123983: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000123983

## Connected records

- collections: [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Acute myeloid leukaemia](https://onco.cc/cancers/aml/)

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JSON: https://onco.cc/api/v1/entities/acsl3.json